S suggest that the OR to develop other types of malignancy
S suggest that the OR to develop other types of malignancy may be decreased, although there were few patients in each of several diagnosis HIV-1 integrase inhibitor 2MedChemExpress HIV-1 integrase inhibitor 2 categories for analysis. We did not study adults with primary central nervous system malignancies, primary gynecologic malignancies (e.g., carcinomas of the endometrium, ovary, or cervix), urothelial malignancies, soft-part sarcomas, primary bone cancers, or Hodgkin disease. Some of these malignancies are uncommon, and some patients are typically not referred to medical oncology and hematology practices. None of the present patients were children. With few exceptions [6,25,47], the relationship of common HFE mutations to neoplasia in childhood has not been reported. It is possible that patients with earlier stages of carcinoma at diagnosis may have different frequencies of C282Y or H63D than persons with similar malignancies that were more advanced at diagnosis. However, this is unlikely in patients with colon and rectal cancer [15]. There is variability in the frequency of HFE alleles and HFE genotypes in persons with hemochromatosis in different subpopulations [48-50]. For example, the reported frequency of C282Y PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28212752 in population control subjects in studies of malignancy varies from 0.0140 [8] to 0.0850 (present study) [8,10,15]. The allele frequencies of C282Y and H63D in the central Alabama whites are relatively great (0.0896 and 0.1447, respectively) [16,17]. Thus, a positive or negative association of malignancy with HFE genotype in a population in which the frequency of HFE mutations is relatively high may be due to chance association with other genetic or environmental factors. Contrariwise, a significantly increased relative risk of malignancy may be more readily demonstrated in populations in which C282Y or H63D frequencies are lower [8,29]. Thus, patient age at diagnosis, type of malignancy, expectations of medical management, stage at diagnosis, and race, ethnicity, and population of origin are important potential sources of variability which must be considered in interpreting results of the present and similar reports, and in designing future studies.Page 5 of(page number not for citation purposes)BMC Cancer 2004,http://www.biomedcentral.com/1471-2407/4/It is difficult to compare reports of the prevalence of malignancy in cohorts of putative hemochromatosis heterozygotes characterized by phenotype criteria and family relationships [1-4] to those performed using HFE mutation testing. In epidemiology studies that use data modeling techniques, iron phenotype data are typically adjusted for common disease-related variables that cause abnormal serum iron concentrations, transferrin saturation values, or serum ferritin concentrations values, thus excluding many study subjects from final analysis [2,51]. Phenotypes of hemochromatosis heterozygotes ascertained in HLA-based family studies or in HFE-based studies are quite variable [38,52]. Thus, using phenotype criteria to identify C282Y or H63D heterozygotes is often unreliable. In some studies, presumed hemochromatosis heterozygotes were ascertained only by self-reported kinship to a putative hemochromatosis homozygote in questionnaire surveys [53]. In family-based studies in which HFE mutation or other DNA-based testing is not used, non-paternity is an additional source of error (1.0 ?1.4 non-paternity in American Caucasians) [54,55]. The basis for the putative association of common HFE mutations and malignancy is unknown. Some C282Y heterozygot.